中文摘要：

目的研究氯离子通道在阿霉素诱导的低分化鼻咽癌CNE-2Z细胞凋亡及凋亡性容积减小中的作用。方法采用全细胞膜片钳技术记录氯电流,流式细胞术检测细胞凋亡,活细胞图像分析法检测细胞容积变化。结果 （1）阿霉素诱导CNE-2Z细胞凋亡;（2）阿霉素诱导CNE-2Z细胞发生凋亡性容积减小,细胞外灌流阿霉素2 h,细胞容积减小约10%;（3）阿霉素可激活氯通道,产生一个有较明显外向优势的氯电流;（4）氯通道阻断剂5-nitro-2-（3-phenylpropylamino）-benzoate（NPPB）明显抑制阿霉素诱导的凋亡性容积减小、细胞凋亡和氯电流。结论阿霉素可通过激活氯通道而诱导细胞凋亡,氯通道在阿霉素诱导的鼻咽癌细胞凋亡中发挥重要作用。

英文摘要：

Aim To investigate the roles of chloride channels in the apoptosis and apoptotic volume decrease（ AVD） induced by adriamycin in nasopharyngeal carcinoma CNE-2Z cells. Methods Apoptotic rates were detected by flow cytometry,and the volume changes were measured by the time-lapse live cell imaging technique. The patch clamp technique was used to record whole-cell chloride currents. Results Adriamycin induced apoptosis of CNE-2Z cells. An early apoptotic volume decrease was observed in the cell treated with adriamycin. The cell volume was decreased by about 10% in 2 h. Adriamycin activated a chloride current which showed outward rectification. The chloride channel blocker 5-nitro-2-（ 3-phenylpropylamino）-benzoate（ NPPB） could inhibit the adriamycin-induced chloride currents,apoptosis and prevent cell shrinkage. Conclusions Our findings suggest that adriamycin causes cell apoptosis by activation of chloride channels. Chloride channels may be involved in the apoptosis and apoptotic volume decrease induced by adriamycin in CNE-2Z cells.